Evidence map›Paper›PMID 28526237›Full record

ArticleExperimental cell research2017

Small-molecule inhibition of Wnt signaling abrogates dexamethasone-induced phenotype of primary human trabecular meshwork cells.

Sarah D Ahadome, Chi Zhang, Elizabeth Tannous, James Shen, Jie J Zheng

Open access · greenAbstract read
In one paragraph

Article in Experimental cell research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Long non-coding RNA SNHG11 regulates the Wnt/β-catenin signaling pathway through rho/ROCK in trabecular meshwork cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Neuroinflammation in Primary Open-Angle Glaucoma.Journal of clinical medicine · 2020
    Review
  14. Article
  15. Article
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Sarah D AhadomeStein Eye Institute, Department of Ophthalmology, David Geffen School of Medicine and Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Chi ZhangStein Eye Institute, Department of Ophthalmology, David Geffen School of Medicine and Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Elizabeth TannousStein Eye Institute, Department of Ophthalmology, David Geffen School of Medicine and Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
James ShenScienCell Research Laboratories, Carlsbad, CA 92011, USA.
Jie J ZhengStein Eye Institute, Department of Ophthalmology, David Geffen School of Medicine and Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA. Electronic address: jzheng@jsei.ucla.edu.
Doheny Eye Institute · USScienCell Research Laboratories (United States) · US

Funding

Structural investigation of focal adhesion formation and disassemblyR01GM100909 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ZHENG, JIE J. · 2012 to 2015
$1.5M
NIGMS NIH HHS R01 GM100909
6 · The paper itself

Abstract

Trabecular meshwork (TM) cells are the governing regulators of the TM structure. When the functionality of these cells is impaired, the structure of the TM is perturbed which often results in increased ocular hypertension. High intraocular pressure is the most significant risk factor for steroid-induced glaucoma. Dexamethasone (Dex)-induced phenotype of TM cells is widely utilized as a model system to gain insight into mechanisms underlying damaged TM in glaucoma. In this study, to assess the possible role of abnormal Wnt signaling in steroid-induced glaucoma, we analyzed the effects of small-molecule Wnt signaling modulators on Dex-induced expression extracellular matrix proteins of primary human TM cells. While Dex-treated TM cells exhibited increased collagen and fibronectin expression, we found that Wnt signaling inhibitor 3235-0367 suppressed these Dex-induced effects. We therefore propose that Wnt signaling plays an important role in Dex-mediated impairment of TM cell functions. Moreover, the use of small-molecule Wnt signaling inhibitors to treat TM cells may provide an opportunity of restoring TM tissue in steroid-induced glaucoma.

Indexed as

Cells, CulturedDexamethasoneExtracellular Matrix ProteinsFibronectinsHumansPhenotypeRNA, MessengerTrabecular MeshworkWnt Signaling PathwayDexamethasoneExtracellular Matrix ProteinsFibronectinsRNA, MessengerDexamethasoneGlaucomaTrabecular meshwork cellWnt

Identifiers

PMID28526237
PMCPMC5535738
OpenAlexW2616199787

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.